|1.||Pili, Roberto: 7 articles (08/2014 - 05/2005)|
|2.||Trepel, Jane B: 7 articles (06/2013 - 02/2002)|
|3.||Figg, William D: 7 articles (09/2007 - 05/2004)|
|4.||Sausville, Edward A: 7 articles (04/2007 - 02/2002)|
|5.||Sabnis, Gauri J: 5 articles (08/2015 - 03/2011)|
|6.||Gore, Steven D: 5 articles (04/2014 - 10/2005)|
|7.||Lee, Min-Jung: 5 articles (09/2007 - 01/2004)|
|8.||Sparreboom, Alex: 5 articles (04/2007 - 05/2004)|
|9.||Chumsri, Saranya: 4 articles (08/2015 - 03/2011)|
|10.||Shah, Preeti: 4 articles (08/2015 - 12/2013)|
10/01/2009 - "Principle component analysis revealed a correlation of the anti-tumor efficacy with the sub-clustering of the MS-275 treatment groups in 7 out of 8 models. "
09/15/2004 - "In tumor growth delay studies, the combination of MS-275 and radiation resulted in a greater than additive inhibition of tumor growth as compared with the individual modalities. "
03/01/2015 - "The narrow-spectrum HDAC inhibitor entinostat enhances NKG2D expression without NK cell toxicity, leading to enhanced recognition of cancer cells."
11/01/2014 - "SGI-110 and entinostat therapy reduces lung tumor burden and reprograms the epigenome."
08/01/2012 - "Therefore, these findings extend our understanding of the action of MS-275 in inducing cancer cell death and suggest that it may be a promising clinical chemotherapeutic agent with multiple effects."
|2.||Lung Neoplasms (Lung Cancer)
01/01/2015 - "Entinostat is a selective HDAC inhibitor that has shown anti-neoplastic activity and tolerability in hematologic and solid tumors, including lung cancer. "
01/01/2006 - "The combination index for MS-275 and PD176252 was <0.2, indicating that the compounds are highly synergistic in inhibiting lung cancer cellular growth. "
01/01/2006 - "Using MS-275 and PD176252 together, the ability to inhibit lung cancer cellular growth increased significantly. "
01/15/2011 - "Combination therapy with vidaza and entinostat suppresses tumor growth and reprograms the epigenome in an orthotopic lung cancer model."
01/01/2006 - "MS-275 had little effect on the expression of lung cancer cellular GRP or GRP receptors, but increased expression of transforming growth factor-beta receptor II (TGF-beta RII). "
07/01/2011 - "Combination of 5-AzadC and MS-275 may be a promising treatment strategy for individuals with leukemia in which TP53 is inactivated."
04/01/2007 - "We conducted a phase 1 trial of orally administered MS-275 in 38 adults with advanced acute leukemias. "
07/24/2014 - "In U937 leukemia cells, 2t was more potent than SAHA in inducing apoptosis, and 3i displayed cell differentiation with a potency similar to MS-275. "
01/01/2014 - "As a proof of principle, we present the identification of Entinostat as a candidate drug for the treatment of HOX-TALE-related leukemia."
07/01/2013 - "Ex vivo treatment of leukemic cells, but not age-matched normal bone marrow controls, with Entinostat validated the gene signature and resulted in reduced viability in liquid culture, impaired colony formation, and loss of the leukemia initiating cell. "
04/08/2008 - "These results suggest that VN/66-1 or its combination with MS-275 may be a novel therapy for the treatment of prostate carcinoma."
08/01/2007 - "In transgenic adenocarcinoma of mouse prostate (TRAMP) mice, long-term treatment of MS-275 slowed the progression of prostate carcinomas with significant reduction in cell proliferation. "
12/01/2010 - "Since non-iodide-concentrating thyroid carcinomas represent a therapeutic problem, this study addressed the effects of the HDAC inhibitor MS-275 on thyroid carcinoma cells. "
12/01/2010 - "MS-275 exerts dose-dependent antiproliferative effects including growth arrest, differentiation and apoptosis in some thyroid carcinoma cell lines and might, therefore, be considered for the treatment of anaplastic and non-iodide-concentrating thyroid carcinomas."
06/15/2005 - "Combination treatment with MS-275 and CRA restored retinoid sensitivity in human prostate carcinoma cell lines, and had a greater inhibitory effect on tumor cell growth than single agents in vitro and in vivo. "
|5.||Hepatocellular Carcinoma (Hepatoma)
08/21/2011 - "Combined PTK/ZK and MS-275 were highly effective in this hepatoma model. "
01/01/2013 - "Effects of the epigenetic drug MS-275 on the release and function of exosome-related immune molecules in hepatocellular carcinoma cells."
12/01/2012 - "Trichostatin, SAHA and MS-275 were applied in a rat hepatoma model. "
12/01/2012 - "Hepatoma cells were incubated with the HDAC inhibitors MS-275, SAHA, FK901228 and trichostatin. "
11/01/2008 - "Human hepatoma cell lines Hep3B and HepG2 as well as primary human foreskin fibroblasts as non-malignant controls were cultured under standardized conditions and incubated with increasing concentrations of CYC-202 and MS-275 as single agents and in combination. "
|1.||Histone Deacetylase Inhibitors
|2.||Histone Deacetylases (Histone Deacetylase)
|3.||vorinostat (suberoylanilide hydroxamic acid)
|4.||Azacitidine (5 Azacytidine)
|5.||trichostatin A (A 300)
|6.||Valproic Acid (Valproate, Semisodium)
|7.||N- (2- aminophenyl)- 4- ((4- pyridin- 3- ylpyrimidin- 2- ylamino)methyl)benzamide
|8.||DNA (Deoxyribonucleic Acid)
|10.||Bee Venoms (Bee Venom)
|1.||Heterologous Transplantation (Xenotransplantation)
|3.||Drug Therapy (Chemotherapy)
|4.||Surgical Instruments (Clip)